In Alzheimer's disease (AD), soluble oligomers of amyloid-β (Aβ) are believed to be primary neurotoxic species responsible for early synaptic dysfunction and cognitive decline. The rate of Aβ aggregation is known to be significantly affected in the presence of anionic interfaces such as lipid, fatty acids & other surfactants. Here, we present the effect of saturated non-esterified fatty acids (NEFAs) on the rate of Aβ aggregation. We have observed that NEFAs induce more than one pathway of Aβ aggregation which is dictated by both ratio of Aβ42 : NEFAs as well as NEFAs respective critical micelle concentrations (CMC). More importantly, we observed that irrespective of their carbon chain lengths, NEFAs generate primarily two types of low molecular weight oligomeric species ; a) near CMC concentration, NEFAs increased the rates of Aβ aggregation towards fibril formation that generated 12-18mers, and b) at concentration above CMC, NEFAs failed to show any aggregation and generated 4-5mers, while oligomeric 12-18mers seems to adopt ‘on pathway’ towards fibril formation, the 4-5mers formed via an alternate pathway called ‘off-pathway’ that did not form fibrils. These oligomers generated were characterized using biophysical techniques like thioflavin-T (ThT) fluorescence, immunoblotting, atomic force microscopy (AFM) and circular dichroism (CD). The results from these analyses also showed that these oligomers are generated via two different pathways. All these data are presented and discussed.